Working to Understand Equine Laminitis

Laminitis is likely the end product of an array of disease processes, one researcher says.
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Equine laminitis can be a devastating result of many different disease processes in the horse, including sepsis and endocrinopathies. The two primary types of endocrinopathic laminitis are equine metabolic syndrome (EMS, seen most often in the obese horse), and Cushing’s syndrome (also known as pituitary pars intermedia disorder) in older horses (characterized by high levels of circulating steroids produced by a pituitary tumor). Interestingly, the "target" tissue in the horse for sepsis, equine metabolic syndrome, and Cushing’s syndrome is the digital laminae.

Most likely the main reason the digital laminae are the primary target is because no other soft tissue structure injury or dysfunction will result in the collapse of the musculoskeletal system of the animal; the laminar basal epithelial cells are exposed to incredible forces (supporting the entire weight of the horse).

Septic conditions in the horse that can lead to laminitis include gastrointestinal disease (surgical lesions, diarrhea/enteritis from infectious agents, or carbohydrate overload), retained placenta in the post-foaling broodmare leading to a uterine infection, pleuropneumonia, and any other infection in which enough tissue is compromised to result in systemic effects. In most of these cases, toxins absorbed from Gram-negative bacteria thought to be responsible for systemic problems, such as laminitis. Bacterial infections from other types of organisms can also result in laminitis. Most progress has been made in studying sepsis-related laminitis, as most experimental models for laminitis mimic this condition.

Systemic inflammation leading to inflammatory injury to the laminar tissue has been reported in sepsis-related laminitis in horses. In the laminae, this injury is characterized by adhesion and migration of circulating white blood cells out of the blood vessels into the laminar tissue. This is accompanied by massive increases in expression of inflammatory proteins such as cytokines (a 10-fold to more than 2,000 fold increase in expression) and cyclooxygenase-2 (COX-2, the enzyme targeted by non-steroidal anti-inflammatory drugs such as phenylbutazone or flunixin). These events most likely cause injury to the laminar basal epithelial cells, leading to disruption of their critical cellular events, including adhesion to the underlying matrix. The matrix itself can also be injured by the release of matrix-degrading enzymes by leukocytes, epithelial cells, and other cell types in the laminae

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